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Role of the second disulfide bridge (Cys18-Cys274) in stabilizing the inactive AT1 receptor

  • Renan Paulo Martin , Eliete da Silva Rodrigues , Silvana Aparecida Alves Correa , Suzana Macedo Oliveira , Renato Arruda Mortara , Laerte Oliveira , Clovis Ryuichi Nakaie and Suma Imura Shimuta
Published/Copyright: August 13, 2010
Biological Chemistry
From the journal Volume 391 Issue 10

Abstract

Previous research showed that disruption of the Cys18-Cys274 bond in the angiotensin II (AngII) AT1 receptor mutant (C18S), expressed in CHO cells, causes an increase in the basal activity and attenuation of the maximum response to AngII. In addition, this mutant was mostly intracellularly distributed. Our aim was to investigate whether the intracellular presence of the mutant was due to a constitutive internalization or to a defective maturation of the receptor. The first hypothesis was assessed by pretreating the cells with losartan or [Sar1Leu8]-AngII, specific AT1 receptor antagonists, a maneuver to revert the receptor internalization. The second hypothesis was tested using calnexin, an endoplasmic reticulum marker. We found that treatment with AT1 receptor antagonists causes an increase in the binding ability of the mutant to AngII. Furthermore, whereas the maximum effect is increased, it reduces the enhanced basal levels of IP3. The hypothesis for a lack of maturation of the mutant receptor was ruled out because calnexin was poorly colocalized with the intracellular C18S receptor. Our results suggest that the mutation of the AT1 receptor leads to a conformational structure similar to that of the active mode of the AT1 receptor, favoring its internalization in the absence of the agonist.

Keywords: angiotensin II; AT1 receptor; mutant; SS salt bridge
Corresponding authors ;
Received: 2010-4-14
Accepted: 2010-6-15
Published Online: 2010-08-13
Published in Print: 2010-10-01

©2010 by Walter de Gruyter Berlin New York

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https://doi.org/10.1515/bc.2010.117
Keywords for this article
angiotensin II; AT1 receptor; mutant; SS salt bridge

Articles in the same Issue

  1. Guest Editorial
  2. Highlight: The Biology of Aging: Mechanisms and Intervention
  3. Highlight: 61th Mosbach Colloquium of the GBM ‘The Biology of Aging: Mechanisms and Intervention’
  4. Multiplex analysis of mitochondrial DNA pathogenic and polymorphic sequence variants
  5. The hypoxia-inducible factor HIF-1 functions as both a positive and negative modulator of aging
  6. E. coli hypoxia-inducible factor ArcA mediates lifespan extension in a lipoic acid synthase mutant by suppressing acetyl-CoA synthetase
  7. Glucose homeostasis and insulin sensitivity in growth hormone-transgenic mice: a cross-sectional analysis
  8. PROTEIN STRUCTURE AND FUNCTION
  9. New structural aspects of FKBP38 activation
  10. The neuronal proteins CIPP, Cypin and IRSp53 form a tripartite complex mediated by PDZ and SH3 domains
  11. CELL BIOLOGY AND SIGNALING
  12. Inhibition of interferon-α-induced signaling by hyperosmolarity and hydrophobic bile acids
  13. Role of the second disulfide bridge (Cys18-Cys274) in stabilizing the inactive AT1 receptor
  14. Demonstration of protein absorption in the intestinal epithelium of fish and mice by laser scanning confocal microscopy
  15. Non-genomic action of TCDD to induce inflammatory responses in HepG2 human hepatoma cells and in liver of C57BL/6J mice
  16. PROTEOLYSIS
  17. Amino acid residues modulating the activities of staphylococcal glutamyl endopeptidases
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